The aim of the study is to investigate the mechanism by which inhaled COS causes neurotoxicity. A 12-week study was conducted to evaluate the neurotoxicity of inhaled COS. Rats were exposed for 12 weeks to 0, 200, 300, or 400 ppm COS. A functional observational battery (FOB) was conducted after 6 and 12-wks of exposure. Only minimal behavioral effects were detected in exposed rats at both time points. Brains were collected from perfused rats after 4, 8, and 12 weeks for histological evaluation, and magnetic resonance microscopy (MRM). Lesions were detected in the parietal cortex by both light microscopy and MRM. In addition, MRM detected a more consistent lesion in the posterior colliculus of rats exposed to 300 and 400 ppm COS. Brains were also collected for biochemical measurements after exposure for 4, 8, and 12 weeks. Cytochrome oxidase activity was decreased in a dose-dependent manner in the parietal cortex and the posterior colliculus after 12-weeks of exposure. Electrophysiological tests conducted on rats after 12-weeks of COS exposure support histopathological evidence of injury to the areas of the brain that control auditory processing. Additional studies are in progress to investigate the potential role of carbonic anhydrase in forming a reactive sulfur intermediate.